Evidence map›Paper›PMID 12037677›Full record

ArticleOncogene2002

STAT3 activation is required for interleukin-6 induced transformation in tumor-promotion sensitive mouse skin epithelial cells.

Cheng-Yong Yu, Lihua Wang, Alexander Khaletskiy, William L Farrar, Andrew Larner, Nancy H Colburn, Jian Jian Li

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 31% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 41 citations in OpenAlex.

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  9. Antitumor efficacy of the anti-interleukin-6 (IL-6) antibody siltuximab in mouse xenograft models of lung cancer.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2014
    Article
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  12. HER2-associated radioresistance of breast cancer stem cells isolated from HER2-negative breast cancer cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 1 country.

Cheng-Yong YuLaboratory of Experimental Immunology, National Cancer Institute, National Institutes of Health, Frederick, Maryland, MD 21702, USA.
Lihua Wang
Alexander Khaletskiy
William L Farrar
Andrew Larner
Nancy H Colburn
Jian Jian Li
National Cancer Institute · USCity Of Hope National Medical Center · USCleveland Clinic · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT3, a member of signal transducers and activators of transcription (STATs) originally discovered as mediators in cytokine signaling pathways, plays an active role in oncogenesis. However, the function of STAT3 in signaling multistage carcinogenesis, especially in transformation of tumor-promotion sensitive epithelial cells has not been elucidated. The present study demonstrates that STAT3 is activated in interleukin-6 induced transformation in mouse skin epithelial cells. DNA binding and transcriptional activities of STAT3 were significantly increased by interleukin-6. This induced anchorage-independent transformation in tumor-promotion sensitive JB6 mouse skin P+ cells but not in the resistant variant P- cells. Two forms of dominant negative STAT3 (mutant of transcriptional domain, mF, or DNA-binding domain, mD) were stably transfected into P+ cells. Activation of STAT3 was abolished and importantly, interleukin-6 induced anchorage-independent growth was absent in both mutant STAT3 transfectants. To determine the genes targeted by STAT3, three matrix metalloproteinase proteins linked with carcinogenesis of epithelial cells were analysed. Both basal and interleukin-6 induced expression of collagenase I and stromelysin I, but not gelatinase A, were inhibited in the mutant STAT3 transfectants. Furthermore, transfection of a wild type STAT3 restored STAT3 transactivation and response to interleukin-6 induced transformation in mutant STAT3 transfectants, which up-regulated collagenase I and stromelysin I as well. Together, these results provide the first evidence that STAT3 activation is required in the progression of multistage carcinogenesis of mouse skin epithelial cells, and matrix metalloproteinases are actively involved in STAT3-mediated cell transformation.

Indexed as

AnimalsCells, CulturedCell Transformation, NeoplasticDNADNA-Binding ProteinsEpithelial CellsHumansInterleukin-6LuciferasesMatrix MetalloproteinasesMiceMolecular Sequence DataPrecipitin TestsPromoter Regions, GeneticReverse Transcriptase Polymerase Chain ReactionRNA, MessengerDNADNA-Binding ProteinsInterleukin-6LuciferasesMatrix MetalloproteinasesRNA, MessengerSTAT1 protein, humanStat1 protein, mouseSTAT1 Transcription FactorSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription FactorTrans-ActivatorsTranscription Factor AP-1

Identifiers

PMID12037677
OpenAlexW2060823188

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.